scholarly journals Biomedical Implications of Heavy Metals Induced Imbalances in Redox Systems

2014 ◽  
Vol 2014 ◽  
pp. 1-26 ◽  
Author(s):  
Bechan Sharma ◽  
Shweta Singh ◽  
Nikhat J. Siddiqi
Keyword(s):  
Oxidative Stress ◽  
Heavy Metals ◽  
Associated Factors ◽  
Current Knowledge ◽  
Toxic Metal ◽  
The Body ◽  
Biological Functions ◽  
Synthetic Antioxidants ◽  
Redox Systems ◽  
Carcinogenic Effects

Several workers have extensively worked out the metal induced toxicity and have reported the toxic and carcinogenic effects of metals in human and animals. It is well known that these metals play a crucial role in facilitating normal biological functions of cells as well. One of the major mechanisms associated with heavy metal toxicity has been attributed to generation of reactive oxygen and nitrogen species, which develops imbalance between the prooxidant elements and the antioxidants (reducing elements) in the body. In this process, a shift to the former is termed as oxidative stress. The oxidative stress mediated toxicity of heavy metals involves damage primarily to liver (hepatotoxicity), central nervous system (neurotoxicity), DNA (genotoxicity), and kidney (nephrotoxicity) in animals and humans. Heavy metals are reported to impact signaling cascade and associated factors leading to apoptosis. The present review illustrates an account of the current knowledge about the effects of heavy metals (mainly arsenic, lead, mercury, and cadmium) induced oxidative stress as well as the possible remedies of metal(s) toxicity through natural/synthetic antioxidants, which may render their effects by reducing the concentration of toxic metal(s). This paper primarily concerns the clinicopathological and biomedical implications of heavy metals induced oxidative stress and their toxicity management in mammals.

scholarly journals Metallothionein and Glutathione Content as Biomarkers of Metal Pollution in Mussels and Local Fishermen in Abu Qir Bay, Egypt

2016 ◽  
Vol 6 (12) ◽  
pp. 50-60 ◽  
Author(s):  
Aziza A. Saad ◽  
Amany El-Sikaily ◽  
Hany Kassem
Keyword(s):  
Oxidative Stress ◽  
Heavy Metals ◽  
Metal Pollution ◽  
The Body ◽  
Metal Exposure ◽  
Control Group ◽  
Blood Levels ◽  
Industrial Workers ◽  
High Concentrations ◽  
Abu Qir Bay

Background. When heavy metals accumulate in air, soil, and water, the risk of human exposure increases among industrial workers, as well as in people living near polluted areas. Heavy metals adversely affect a variety of bodily systems such as the cardiovascular, respiratory, endocrine, immune, and reproductive systems. In addition, long-term exposure and accumulation of heavy metals in the body may disturb oxidative stress genes and thus increase the susceptibility to various diseases. Objectives. The aim of this study is to estimate the metallothionein concentration in both mussel samples from Abu Qir Bay, Egypt and the blood of local fishermen as a biomarker of exposure to metal pollution. Methods. Levels of metallothionein and heavy metals were measured in mussels. Blood levels of metallothionein and heavy metals of local fishermen were measured and compared with a control group. The effect of heavy metal exposure on oxidative stress status was investigated through the determination of malondialdehyde (MDA), catalase and glutathione content. Results. The results of this study showed high concentrations of metallothionein in mussels and in fishermen's blood, accompanied by high concentrations of metals such as cadmium (Cd), copper (Cu), lead (Pb), chromium (Cr), and zinc (Zn). At the same time, a significant decrease in glutathione content and catalase enzyme activity was associated with a significant increase in the malondialdehyde concentrations in sera of fishermen. Conclusions. The present study found that the El Maadiya region is polluted with heavy metals, inducing oxidative stress in fishermen in the vicinity. These results reveal the necessity of further environmental monitoring in the study area in order to evaluate other types of pollutants and their effects on human health.

scholarly journals Regulation of the Proteolytic Activity of Cysteine Cathepsins by Oxidants

2020 ◽  
Vol 21 (6) ◽  
pp. 1944 ◽  
Author(s):  
Gilles Lalmanach ◽  
Ahlame Saidi ◽  
Paul Bigot ◽  
Thibault Chazeirat ◽  
Fabien Lecaille ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Molecular Mechanisms ◽  
Current Knowledge ◽  
Sulfhydryl Group ◽  
Redox Balance ◽  
Biological Functions ◽  
Cysteine Cathepsins ◽  
Michael Acceptors ◽  
Natural Inhibitors

Besides their primary involvement in the recycling and degradation of proteins in endo-lysosomal compartments and also in specialized biological functions, cysteine cathepsins are pivotal proteolytic contributors of various deleterious diseases. While the molecular mechanisms of regulation via their natural inhibitors have been exhaustively studied, less is currently known about how their enzymatic activity is modulated during the redox imbalance associated with oxidative stress and their exposure resistance to oxidants. More specifically, there is only patchy information on the regulation of lung cysteine cathepsins, while the respiratory system is directly exposed to countless exogenous oxidants contained in dust, tobacco, combustion fumes, and industrial or domestic particles. Papain-like enzymes (clan CA, family C1, subfamily C1A) encompass a conserved catalytic thiolate-imidazolium pair (Cys25-His159) in their active site. Although the sulfhydryl group (with a low acidic pKa) is a potent nucleophile highly susceptible to chemical modifications, some cysteine cathepsins reveal an unanticipated resistance to oxidative stress. Besides an introductory chapter and peculiar attention to lung cysteine cathepsins, the purpose of this review is to afford a concise update of the current knowledge on molecular mechanisms associated with the regulation of cysteine cathepsins by redox balance and by oxidants (e.g., Michael acceptors, reactive oxygen, and nitrogen species).

scholarly journals Impact of Lifestyles (Diet and Exercise) on Vascular Health: Oxidative Stress and Endothelial Function

2020 ◽  
Vol 2020 ◽  
pp. 1-22 ◽  
Author(s):  
Andy W. C. Man ◽  
Huige Li ◽  
Ning Xia
Keyword(s):  
Oxidative Stress ◽  
Metabolic Diseases ◽  
Healthy Lifestyle ◽  
Current Knowledge ◽  
Vascular Dysfunction ◽  
The Body ◽  
Physical Factors ◽  
Normal Functions ◽  
The Impact ◽  
And Oxidative Stress

Healthy lifestyle and diet are associated with significant reduction in risk of obesity, type 2 diabetes, and cardiovascular diseases. Oxidative stress and the imbalance between prooxidants and antioxidants are linked to cardiovascular and metabolic diseases. Changes in antioxidant capacity of the body may lead to oxidative stress and vascular dysfunction. Diet is an important source of antioxidants, while exercise offers many health benefits as well. Recent findings have evidenced that diet and physical factors are correlated to oxidative stress. Diet and physical factors have debatable roles in modulating oxidative stress and effects on the endothelium. Since endothelium and oxidative stress play critical roles in cardiovascular and metabolic diseases, dietary and physical factors could have significant implications on prevention of the diseases. This review is aimed at summarizing the current knowledge on the impact of diet manipulation and physical factors on endothelium and oxidative stress, focusing on cardiovascular and metabolic diseases. We discuss the friend-and-foe role of dietary modification (including different diet styles, calorie restriction, and nutrient supplementation) on endothelium and oxidative stress, as well as the potential benefits and concerns of physical activity and exercise on endothelium and oxidative stress. A fine balance between oxidative stress and antioxidants is important for normal functions in the cells and interfering with this balance may lead to unfavorable effects. Further studies are needed to identify the best diet composition and exercise intensity.

scholarly journals An Evaluation of the Clinical Evidence on the Role of Inflammation and Oxidative Stress in Smoking-Mediated Cardiovascular Disease

2008 ◽  
Vol 3 ◽  
pp. BMI.S480 ◽  
Author(s):  
Adam Csordas ◽  
Georg Wick ◽  
Günther Laufer ◽  
David Bernhard
Keyword(s):  
Oxidative Stress ◽  
Heavy Metals ◽  
Cardiovascular Disease ◽  
Primary Prevention ◽  
Human Life ◽  
Large Population ◽  
Basic Research ◽  
High Sensitivity ◽  
The Body ◽  
Prevention Strategies

The number of fatalities due to cardiovascular disease (CVD) continues to be far ahead of loss of human life caused by any other type of disease worldwide. According to the WHO, the annual global tobacco death toll is already 8.4 million and will reach 10 million by the year 2025. However, in contrast to other modifiable primary risk factors for CVD such as obesity, primary prevention strategies for smokers unable to quit are not available to date. This Review, by adopting the principles of evidence-based medicine, summarizes the most recent clinical studies on CVD in smokers, and concludes by suggesting a novel primary prevention strategy for CVD in smokers unable to quit. Evidence gathered from mechanistic studies involving basic research as well as large population-based approaches point to oxidative stress as the major insult imposed by cigarette smoke (CS), and a state of systemic inflammation, as signified by increased hs (high sensitivity) CRP levels in smokers, as the decisive pro-atherogenic response of the body to the initial insult. Since we identified oxidative stress induced by heavy metals as a significant pro-atherogenic activity of CS, strategies aimed at detoxifying heavy metals and combating inflammation appear as plausible approaches to counteract the accelerated onset of CVD in smokers. For this purpose, we discuss metal chelating agents and statins as promising novel primary prevention strategies in smokers unable to quit.

scholarly journals Toxic Mechanisms of Five Heavy Metals: Mercury, Lead, Chromium, Cadmium, and Arsenic

2021 ◽  
Vol 12 ◽  
Author(s):  
Mahdi Balali-Mood ◽  
Kobra Naseri ◽  
Zoya Tahergorabi ◽  
Mohammad Reza Khazdair ◽  
Mahmood Sadeghi
Keyword(s):  
Oxidative Stress ◽  
Heavy Metals ◽  
Aminolevulinic Acid ◽  
Current Knowledge ◽  
Enzyme Inactivation ◽  
Ros Generation ◽  
Defense Enzyme ◽  
Cellular Events ◽  
Body Tissues ◽  
Antioxidant Defense Enzyme

The industrial activities of the last century have caused massive increases in human exposure to heavy metals. Mercury, lead, chromium, cadmium, and arsenic have been the most common heavy metals that induced human poisonings. Here, we reviewed the mechanistic action of these heavy metals according to the available animal and human studies. Acute or chronic poisonings may occur following exposure through water, air, and food. Bioaccumulation of these heavy metals leads to a diversity of toxic effects on a variety of body tissues and organs. Heavy metals disrupt cellular events including growth, proliferation, differentiation, damage-repairing processes, and apoptosis. Comparison of the mechanisms of action reveals similar pathways for these metals to induce toxicity including ROS generation, weakening of the antioxidant defense, enzyme inactivation, and oxidative stress. On the other hand, some of them have selective binding to specific macromolecules. The interaction of lead with aminolevulinic acid dehydratase and ferrochelatase is within this context. Reactions of other heavy metals with certain proteins were discussed as well. Some toxic metals including chromium, cadmium, and arsenic cause genomic instability. Defects in DNA repair following the induction of oxidative stress and DNA damage by the three metals have been considered as the cause of their carcinogenicity. Even with the current knowledge of hazards of heavy metals, the incidence of poisoning remains considerable and requires preventive and effective treatment. The application of chelation therapy for the management of metal poisoning could be another aspect of heavy metals to be reviewed in the future.

scholarly journals Regulation of the Proteolytic Activity of Cysteine Cathepsins by Oxidants

2020 ◽  
Author(s):  
Gilles Lalmanach ◽  
Ahlame Saidi ◽  
Paul Bigot ◽  
Thibault Chazeirat ◽  
Fabien Lecaille ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Molecular Mechanisms ◽  
Current Knowledge ◽  
Sulfhydryl Group ◽  
Redox Balance ◽  
Biological Functions ◽  
Cysteine Cathepsins ◽  
Michael Acceptors ◽  
Natural Inhibitors

Besides their primary involvement in the recycling and degradation of proteins in endo-lysosomal compartments but also in specialized biological functions, cysteine cathepsins are pivotal proteolytic contributors of various deleterious diseases. While the molecular mechanisms of regulation by their natural inhibitors have been exhaustively studied, less is currently known about how their enzymatic activity is modulated during the redox imbalance associated with an oxidative stress and their exposure resistance to oxidants. More specifically, there is only patchy information on the regulation of lung cysteine cathepsins, while the respiratory system is directly exposed to countless exogenous oxidants contained in dust, tobacco, combustion fumes, and industrial or domestic particles. Papain-like enzymes (clan CA, family C1, subfamily C1A) encompass a conserved catalytic thiolate-imidazolium pair (Cys25-His159) in their active site. Despite the sulfhydryl group (with a low acidic pKa) is a potent nucleophile highly susceptible to chemical modifications, some cysteine cathepsins reveal an unanticipated resistance to oxidative stress. Beside an introductory chapter and a peculiar attention to lung cysteine cathepsins, the purpose of this review is to afford a concise update of the current knowledge on molecular mechanisms associated to the regulation of cysteine cathepsins by redox balance and by oxidants (e.g. Michael acceptors, reactive oxygen and nitrogen species).

scholarly journals Antioxidants level assessment in the diet of workers contacting with heavy metals at industrial enterprise

2019 ◽  
Vol 95 (2) ◽  
pp. 165-167
Author(s):  
T. V. Mazhaeva ◽  
Svetlana E. Dubenko ◽  
I. A. Chirkova
Keyword(s):  
Oxidative Stress ◽  
Heavy Metals ◽  
Heavy Metal ◽  
Toxic Effect ◽  
Quantitative Assessment ◽  
The Body ◽  
Oxidation Reactions ◽  
Brown Bread ◽  
High Level ◽  
Low Activity

The main occupational pathologies in the Sverdlovsk region are diseases induced by the exposure to industrial aerosols containing heavy metals. One of the reasons of the toxic effect of the heavy metals is oxidative stress induced by the latter, namely, the process of damaging the body cells as a result of the oxidation reactions. The quantitative assessment of the antioxidant consumption in foods composing the diet of heavy metal industry workers was performed. The diet was revealed to be not various in terms of the foods containing antioxidants and the main quantity of the latter was administered into the body from the brown bread, tea, apples, chocolates and sweets having low activity according to the ORAC index but consumed in the great amounts. In the meantime, foods with the high level of the antioxidant content and bio-correction properties (fruits, vegetables, spices) were lacking in the diet and this fact could probably influence on the decline of the body’s reserve of detoxification.

Lead-induced oxidative stress adversely affects health of the occupational workers

2008 ◽  
Vol 24 (9) ◽  
pp. 611-618 ◽  
Author(s):  
DA Khan ◽  
S Qayyum ◽  
S Saleem ◽  
FA Khan
Keyword(s):  
Oxidative Stress ◽  
Uric Acid ◽  
Biochemical Markers ◽  
Lead Level ◽  
Toxic Metal ◽  
Blood Lead ◽  
The Body ◽  
Industrial Workers ◽  
Positive Correlation ◽  
Exposed Workers

Lead is a persistent toxic metal and associated with impairment of various body functions in occupational workers. The main objective was to determine the lead-induced oxidative stress and adverse health effects by biochemical markers in industrial workers. One hundred and forty-eight males consisting of 87 lead-exposed industrial workers and 61 controls were included. Blood lead level (BLL) was determined on a 3010B ESA lead analyzer. Blood complete counts were done on a hematology analyzer. Biochemical markers including serum uric acid, urea, creatinine, phosphate, alanine aminotransferase (ALT), and gamma glutamyltransferase (GGT) were measured on a Selectra E auto analyzer. Serum malondialdehyde (MDA) was measured spectrophotometrically and C-reactive protein (CRP) on Immulite-1000. Results revealed that lead-exposed workers had significantly high BLLs, median (range), 29.1 (9.0–61.1) μg/dL compared with controls, 8.3 (1.0–21.7) μg/dL. Oxidative stress (MDA, GGT) and inflammatory markers (high-sensitivity CRP) were significantly increased ( P ≤ 0.05). Blood pressure was raised, whereas hemoglobin was decreased in exposed group ( P ≤ 0.002). Serum urea, uric acid, phosphate, and ALT were significantly raised in lead-exposed workers ( P ≤ 0.001). Serum albumin, total proteins, and glomerular filtration rate (GFR) were decreased. Blood lead showed a significant positive correlation with serum GGT ( r = 0.63), MDA ( r = 0.71), CRP ( r = 0.75), urea ( r = 0.34), creatinine ( r = 0.51), and uric acid ( r = 0.29) ( P ≤ 0.01). It is concluded that lead exposure increases oxidative stress that correlates with adverse changes in hematological, renal, and hepatic function in the occupational workers. Elevated blood lead has positive correlation with oxidative stress, inflammatory and biochemical markers that might be used to detect impairment in the body function in lead exposed workers.

scholarly journals Genetic engineering of mesenchymal stromal cells for cancer therapy: turning partners in crime into Trojan horses

2016 ◽  
Vol 1 (1) ◽  
pp. 19-32 ◽  
Author(s):  
Hanno Niess ◽  
Michael N. Thomas ◽  
Tobias S. Schiergens ◽  
Axel Kleespies ◽  
Karl-Walter Jauch ◽  
...  
Keyword(s):  
Mesenchymal Stromal Cells ◽  
Stromal Cells ◽  
Current Knowledge ◽  
Cell Types ◽  
The Body ◽  
Biological Functions ◽  
Connective Tissues ◽  
Differentiation Potential ◽  
Underlying Mechanisms ◽  
Do So

AbstractMesenchymal stromal cells (MSCs) are adult progenitor cells with a high migratory and differentiation potential, which influence a broad range of biological functions in almost every tissue of the body. Among other mechanisms, MSCs do so by the secretion of molecular cues, differentiation toward more specialized cell types, or influence on the immune system. Expanding tumors also depend on the contribution of MSCs to building a supporting stroma, but the effects of MSCs appear to go beyond the mere supply of connective tissues. MSCs show targeted “homing” toward growing tumors, which is then followed by exerting direct and indirect effects on cancer cells. Several research groups have developed novel strategies that make use of the tumor tropism of MSCs by engineering them to express a transgene that enables an attack on cancer growth. This review aims to familiarize the reader with the current knowledge about MSC biology, the existing evidence for MSC contribution to tumor growth with its underlying mechanisms, and the strategies that have been developed using MSCs to deploy an anticancer therapy.

scholarly journals Physiology of magnesium metabolism and the use of magnesium in intensive care (part 2)

2021 ◽  
Vol 17 (6) ◽  
pp. 17-27
Author(s):  
S.V. Kursov ◽  
V.V. Nikonov ◽  
O.V. Biletskyi ◽  
O.E. Feskov ◽  
S.M. Skoroplit
Keyword(s):  
Oxidative Stress ◽  
Heavy Metals ◽  
Organophosphorus Compounds ◽  
Stress Hormones ◽  
The Body ◽  
High Rate ◽  
Critical Conditions ◽  
Pathological Effect ◽  
Free Radical Damage ◽  
Magnesium Metabolism

In the second part of the review, aspects of changes in magnesium metabolism under conditions of severe stress, mechanisms of anti-stress protection of the body with the participation of magnesium, features of magnesium participation in water-electrolyte metabolism at the cellular level, the anti-inflammatory effect of magnesium and the role of magnesium in the processes of detoxification of the body in acute poisoning with certain poisons are consi-dered. The main mechanisms of the body’s magnesium defence are to suppress the mechanisms of oxidative stress by limiting the production of stress hormones, the intake of ionized calcium and sodium into cells with a decrease in the severity of transmineralization and sodium retention in the body, suppressing the action of factors that initiate the development of inflammation and reducing the production of pro-inflammatory mediators, in blocking and protecting glutamate receptors. Magnesium therapy can help keep effective energy production in the body in critical conditions by maintaining the functioning of the Na+/K+-ATPase, the work of the Na+/H+-exchanger, helping reduce the severity of cellular acidosis. The mechanisms of functioning and the prescription of the sodium-magnesium antiporter are discussed. Hypertonic solutions of magnesium sulfate are being injected at a high rate to create the effect of rapid low-volume fluid resuscitation, thereby eliminating the dangerous effects of severe hyperchloremia and hypernatremia that occur when using hypertonic sodium chloride solutions. In toxico-logy, magnesium preparations are used to protect the body when exposed to heavy metals, organophosphorus compounds. They also help reduce the severity of oxidative stress caused by heavy metals, inhibit excess production of endogenous carbon monoxide, and limit free radical damage in its pathological effect. During detoxification, magnesium prevents depletion of the antioxidant system by helping maintain sufficient levels of glutathione and other antioxidants in cells.

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